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Clonal evolution and clinical correlates of somatic mutations in myeloproliferative neoplasms

Blood, 2014-04, Vol.123 (14), p.2220-2228

2014

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Pathogenesis of myeloproliferative neoplasms

Experimental hematology, 2015-08, Vol.43 (8), p.599-608

2015

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Neuropathy of haematopoietic stem cell niche is essential for myeloproliferative neoplasms

Nature (London), 2014-08, Vol.512 (7512), p.78-81

2014

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Estrogen Signaling Selectively Induces Apoptosis of Hematopoietic Progenitors and Myeloid Neoplasms without Harming Steady-State Hematopoiesis

Cell stem cell, 2014-12, Vol.15 (6), p.791-804

2014

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Loss of EZH2 Reprograms BCAA Metabolism to Drive Leukemic Transformation

Cancer discovery, 2019-09, Vol.9 (9), p.1228-1247

2019

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Pf4-Cre transgenic mice allow the generation of lineage-restricted gene knockouts for studying megakaryocyte and platelet function in vivo

Blood, 2007-02, Vol.109 (4), p.1503-1506

2007

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Inhibition of interleukin-1β reduces myelofibrosis and osteosclerosis in mice with JAK2-V617F driven myeloproliferative neoplasm

Nature communications, 2022-09, Vol.13 (1), p.5346-14, Article 5346

2022

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Clonal hematopoiesis in donors and long-term survivors of related allogeneic hematopoietic stem cell transplantation

Blood, 2020-04, Vol.135 (18), p.1548-1559

2020

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ATP binding to the pseudokinase domain of JAK2 is critical for pathogenic activation

Proceedings of the National Academy of Sciences - PNAS, 2015-04, Vol.112 (15), p.4642-4647

2015

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Ratio of mutant JAK2-V617F to wild-type Jak2 determines the MPD phenotypes in transgenic mice

Blood, 2008-04, Vol.111 (8), p.3931-3940

2008

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Ruxolitinib-induced defects in DNA repair cause sensitivity to PARP inhibitors in myeloproliferative neoplasms

Blood, 2017-12, Vol.130 (26), p.2848-2859

2017

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Mouse models of myeloproliferative neoplasms for pre-clinical testing of novel therapeutic agents

Biomedical papers of the Medical Faculty of the University Palacký, Olomouc, Czechoslovakia, 2021-03, Vol.165 (1), p.26-33

2021

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Deletion of Stat3 in hematopoietic cells enhances thrombocytosis and shortens survival in a JAK2-V617F mouse model of MPN

Blood, 2015-03, Vol.125 (13), p.2131-2140

2015

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Leukemic blasts in transformed JAK2-V617F–positive myeloproliferative disorders are frequently negative for the JAK2-V617F mutation

Blood, 2007-07, Vol.110 (1), p.375-379

2007

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Genetic basis and molecular profiling in myeloproliferative neoplasms

Blood, 2023-04, Vol.141 (16), p.1909-1921

2023

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Talin is required for integrin-mediated platelet function in hemostasis and thrombosis

The Journal of experimental medicine, 2007-12, Vol.204 (13), p.3103-3111

2007

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Loss of Stat1 decreases megakaryopoiesis and favors erythropoiesis in a JAK2-V617F–driven mouse model of MPNs

Blood, 2014-06, Vol.123 (25), p.3943-3950

2014

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JAK2 impairs stem cell function?

Blood, 2010-09, Vol.116 (9), p.1392-1393

Skoda, Radek C.

2010

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The DEAH-box helicase RHAU is an essential gene and critical for mouse hematopoiesis

Blood, 2012-05, Vol.119 (18), p.4291-4300

2012

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Biphasic roles for soluble guanylyl cyclase (sGC) in platelet activation

Blood, 2011-09, Vol.118 (13), p.3670-3679

2011

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Accelerating myelofibrosis through loss of Dnmt3a

Blood, 2018-12, Vol.132 (26), p.2703-2704

Skoda, Radek C.

2018

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Dual roles of EZH2 in acute myeloid leukemia

The Journal of experimental medicine, 2019-04, Vol.216 (4), p.725-727

2019

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Remodeling of metabolism and inflammation by exercise ameliorates tumor-associated anemia

Science advances, 2021-09, Vol.7 (37), p.eabi4852-eabi4852

2021

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Longitudinal Cytokine Profiling Identifies GRO‐α and EGF as Potential Biomarkers of Disease Progression in Essential Thrombocythemia

HemaSphere, 2020-06, Vol.4 (3), p.e371-n/a

2020

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Clonal evolution and clinical correlates of somatic mutations in myeloproliferative neoplasms

Pathogenesis of myeloproliferative neoplasms

Neuropathy of haematopoietic stem cell niche is essential for myeloproliferative neoplasms

Estrogen Signaling Selectively Induces Apoptosis of Hematopoietic Progenitors and Myeloid Neoplasms without Harming Steady-State Hematopoiesis

Loss of EZH2 Reprograms BCAA Metabolism to Drive Leukemic Transformation

Pf4-Cre transgenic mice allow the generation of lineage-restricted gene knockouts for studying megakaryocyte and platelet function in vivo

Inhibition of interleukin-1β reduces myelofibrosis and osteosclerosis in mice with JAK2-V617F driven myeloproliferative neoplasm

Clonal hematopoiesis in donors and long-term survivors of related allogeneic hematopoietic stem cell transplantation

ATP binding to the pseudokinase domain of JAK2 is critical for pathogenic activation

Ratio of mutant JAK2-V617F to wild-type Jak2 determines the MPD phenotypes in transgenic mice

Ruxolitinib-induced defects in DNA repair cause sensitivity to PARP inhibitors in myeloproliferative neoplasms

Mouse models of myeloproliferative neoplasms for pre-clinical testing of novel therapeutic agents

Deletion of Stat3 in hematopoietic cells enhances thrombocytosis and shortens survival in a JAK2-V617F mouse model of MPN

Leukemic blasts in transformed JAK2-V617F–positive myeloproliferative disorders are frequently negative for the JAK2-V617F mutation

Genetic basis and molecular profiling in myeloproliferative neoplasms

The sympathomimetic agonist mirabegron did not lower JAK2 -V617F allele burden, but restored nestin-positive cells and reduced reticulin fibrosis in patients with myeloproliferative neoplasms: results of phase II study SAKK 33/14

Talin is required for integrin-mediated platelet function in hemostasis and thrombosis

Loss of Stat1 decreases megakaryopoiesis and favors erythropoiesis in a JAK2-V617F–driven mouse model of MPNs

JAK2 impairs stem cell function?

The DEAH-box helicase RHAU is an essential gene and critical for mouse hematopoiesis

Biphasic roles for soluble guanylyl cyclase (sGC) in platelet activation

Accelerating myelofibrosis through loss of Dnmt3a

Dual roles of EZH2 in acute myeloid leukemia

Remodeling of metabolism and inflammation by exercise ameliorates tumor-associated anemia

Longitudinal Cytokine Profiling Identifies GRO‐α and EGF as Potential Biomarkers of Disease Progression in Essential Thrombocythemia

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